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      Electrocardiographic Left Ventricular Hypertrophy Predicts Cardiovascular Morbidity and Mortality in Hypertensive Patients: The ALLHAT Study

      1 , 2 , 3 , 4 , 4 , 1 , 1 , and for the ALLHAT Collaborative Research Group
      American Journal of Hypertension
      Oxford University Press (OUP)

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          Abstract

          <div class="section"> <a class="named-anchor" id="d7571860e228"> <!-- named anchor --> </a> <h5 class="section-title" id="d7571860e229">BACKGROUND</h5> <p id="d7571860e231">Electrocardiographic (ECG) left ventricular hypertrophy (LVH) is a strong predictor of cardiovascular (CV) morbidity and mortality. However, the predictive value of ECG LVH in treated hypertensive patients remains unclear. </p> </div><div class="section"> <a class="named-anchor" id="d7571860e233"> <!-- named anchor --> </a> <h5 class="section-title" id="d7571860e234">METHODS</h5> <p id="d7571860e236">A total of 33,357 patients (aged ≥ 55 years) with hypertension and at least 1 other coronary heart disease (CHD) risk factor were randomized to chlorthalidone, amlodipine, or lisinopril. The outcome of the present study was all-cause mortality; and secondary endpoints were CHD, nonfatal myocardial infarction (MI), stroke, angina, heart failure (HF), and peripheral arterial disease. Cornell voltage criteria (S in V <sub>3</sub> + R in aVL &gt; 28 [men] or &gt;22 mm [women]) defined ECG LVH. </p> </div><div class="section"> <a class="named-anchor" id="d7571860e241"> <!-- named anchor --> </a> <h5 class="section-title" id="d7571860e242">RESULTS</h5> <p id="d7571860e244">ECGs were available at baseline in 26,384 patients. Baseline Cornell voltage LVH was present in 1,741 (7%) patients, who were older (67.4 vs. 66.6 years, <i>P</i> &lt; 0.001), more likely to be female (74 vs. 44%, <i>P</i> &lt; 0001) with a higher systolic blood pressure (151 vs. 146 mm Hg, <i>P</i> &lt; 0.001) than patients without ECG LVH. During 5.0 ± 1.4 years mean follow-up, baseline and in-study ECG LVH was significantly associated with 29 to 98% increased risks of all-cause mortality, MI, CHD, stroke, and HF in multivariable Cox analyses. </p> </div><div class="section"> <a class="named-anchor" id="d7571860e255"> <!-- named anchor --> </a> <h5 class="section-title" id="d7571860e256">CONCLUSIONS</h5> <p id="d7571860e258">Baseline Cornell voltage LVH is associated with increased CV morbidity and all-cause mortality in treated hypertensive patients independent of treatment modality and other CV risk factors. </p> </div><div class="section"> <a class="named-anchor" id="d7571860e260"> <!-- named anchor --> </a> <h5 class="section-title" id="d7571860e261">CLINICAL TRIALS REGISTRATION</h5> <p id="d7571860e263">Trial Number NCT00000542.</p> </div>

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          Most cited references15

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          Major Cardiovascular Events in Hypertensive Patients Randomized to Doxazosin vs Chlorthalidone: The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT)

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            Reduction of cardiovascular risk by regression of electrocardiographic markers of left ventricular hypertrophy by the angiotensin-converting enzyme inhibitor ramipril.

            Electrocardiographic markers of left ventricular hypertrophy (LVH) predict poor prognosis. We determined whether the ACE inhibitor ramipril prevents the development and causes regression of ECG-LVH and whether these changes are associated with improved prognosis independent of blood pressure reduction. In the Heart Outcomes Prevention Evaluation (HOPE) study, patients at high risk were randomly assigned to ramipril or placebo and followed for 4.5years. ECGs were recorded at baseline and at study end. We compared prevention/regression and development/persistence of ECG-LVH in the two groups and related these changes to outcomes. At baseline, 676 patients had LVH (321 in the ramipril group and 355 in the placebo group) and 7605 patients did not have LVH (3814 in the ramipril group and 3791 in the placebo group). By study end, 336 patients in the ramipril group (8.1%) compared with 406 in the placebo group (9.8%) had development/persistence of LVH; in contrast, 3799 patients in the ramipril group (91.9%) compared with 3740 in the placebo group (90.2%) had regression/prevention of LVH (P=0.007). The effect of ramipril on LVH was independent of blood pressure changes. Patients who had regression/prevention of LVH had a lower risk of the predefined primary outcome (cardiovascular death, myocardial infarction, or stroke) compared with those who had development/persistence of LVH (12.3% versus 15.8%, P=0.006) and of congestive heart failure (9.3% versus 15.4%, P<0.0001). The ACE inhibitor ramipril decreases the development and causes regression of ECG-LVH independent of blood pressure reduction, and these changes are associated with reduced risk of death, myocardial infarction, stroke, and congestive heart failure.
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              Prognostic implications of baseline electrocardiographic features and their serial changes in subjects with left ventricular hypertrophy.

              During the past half-century, the ECG has been used extensively for the diagnosis of left ventricular hypertrophy. Persons with ECG evidence of left ventricular hypertrophy are at increased risk for the development of cardiovascular disease. Subjects from the Framingham Heart Study with ECG evidence of left ventricular hypertrophy were eligible for this investigation if they were free of cardiovascular disease and did not have complete bundle-branch block or Wolff-Parkinson-White syndrome. Logistic regression analyses of pooled biennial examinations were used to determine risk for cardiovascular disease as a function of baseline voltage (sum of R wave in aVL plus S wave in V3) and repolarization and as a function of serial changes in these ECG features of hypertrophy. The eligible sample consisted of 274 men (mean age, 60 years) and 250 women (mean age, 64 years) who contributed 2660 person-examinations. During follow-up, there were 269 new cardiovascular events. Compared with subjects in the first quartile of voltage at baseline, the age-adjusted odds ratio for cardiovascular disease among subjects in the fourth quartile was 3.08 (95% confidence interval [CI], 1.87 to 5.07) in men and 3.29 (95% CI, 1.78 to 6.09) in women. Compared with a normal repolarization pattern, the presence of severe repolarization abnormalities was associated with an age-adjusted odds ratio of 5.84 (95% CI, 3.55 to 9.62) in men and 2.47 (95% CI, 1.38 to 4.42) in women. Subjects with a serial decline in voltage were at lower risk for cardiovascular disease than were those with no serial change (men: odds ratio after adjusting for age and baseline voltage, 0.46; 95% CI, 0.26 to 0.84; women: odds ratio, 0.56; 95% CI, 0.30 to 1.04). In contrast, those with a serial increase in voltage were at greater risk for cardiovascular disease (men: odds ratio, 1.86; 95% CI, 1.14 to 3.03; women: odds ratio, 1.61; 95% CI, 0.91 to 2.84). Compared with those with no serial change, an improvement in repolarization was associated with a marginally significant reduction in cardiovascular risk in men (odds ratio after adjusting for age and baseline repolarization, 0.45; 95% CI, 0.20 to 1.01). Worsening of repolarization was associated with increased risk for cardiovascular disease in both sexes (men: odds ratio, 1.89; 95% CI, 1.05 to 3.40; women: odds ratio, 2.02; 95% CI, 1.07 to 3.81). The results of this investigation suggest that regression of ECG features of left ventricular hypertrophy confers an improvement in risk for cardiovascular disease, whereas serial worsening imposes increased risk. The benefits to be derived from regression of left ventricular hypertrophy must be confirmed in other clinical settings.
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                Author and article information

                Journal
                American Journal of Hypertension
                Oxford University Press (OUP)
                0895-7061
                1941-7225
                September 2017
                September 01 2017
                April 19 2017
                September 2017
                September 01 2017
                April 19 2017
                : 30
                : 9
                : 914-922
                Affiliations
                [1 ] Division of Cardiology, Department of Medicine, Weill Cornell Medical College, New York, New York, USA;
                [2 ] Department of Cardiology, Zealand University Hospital Roskilde, Roskilde, Denmark;
                [3 ] Epidemiological Cardiology Research Center (EPICARE), Division of Public Health Sciences, Section of Cardiology, Department of Medicine, Wake Forest School of Medicine, Winston Salem, North Carolina, USA;
                [4 ] Department of Biostatistics|Coordinating Center for Clinical Trials, School of Public Health, The University of Texas Health Science Center at Houston, Houston, Texas, USA.
                Article
                10.1093/ajh/hpx067
                5861536
                28430947
                7ed8425a-316f-48d5-95d5-048b2cbcff7b
                © 2017
                History

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